Current EITS Students

Learn more about the research interests of our current EITS students by selecting their name below.

 

Biochemistry and Molecular Biology

  • Warren Sink

    Warren SinkCooperating Doctoral Program: Cell and Molecular Biology

    EITS Track: Biomedical Toxicology

    Education: B.S. Cell and Molecular Biology, Grand Valley State University

    Research Interests:
    My proposed doctoral research includes (1) the utilization of mouse thermoneutral studies to assess the progression of toxicant associated fatty liver disease (TAFLD) with broad implications of human nonalcoholic fatty liver disease (NAFLD) progression. Standard mouse toxicology studies are conducted at human thermoneutral temperatures (20 – 23°C) leading to unwarranted cold stress. By investigating the toxicological effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) at 29 – 32°C, the progression of toxicant-induced liver disease is expected to mimic that more closely to human NAFLD pathologies. Work from my doctoral project with will include a collaboration with Dr. Arjun Krishan's lab (Computational Mathematics, Science and Engineering department) to employ (2) the application of contemporary data science techniques to integrate experimental datasets produced from -omic experiments, such as (but not limited to) RNA-seq, ChIP-seq, and metabolomics. Data generated as part of my project will (3) adhere to the implementation of Findable, Accessible, Interoperable, and Reusable (FAIR) guidelines by coordinating with the Data Management and Analysis (DMAC) core. These datasets will be further developed with the web-based application FAIRtox to provide researchers and the public the opportunity to interact with dose-dependent toxicological RNA-seq data, ChIP-seq, and, in the future, other -omic datasets.

    Major Professor: Timothy Zacharewski, Biochemistry and Molecular Biology

    Contact: sinkwarr@msu.edu

Chemistry

  • Jennifer Hinman

    Jennifer HinmanCooperating Doctoral Program: Chemistry

    EITS Track: Biomedical Toxicology

    Education: B.S. Chemistry, B.A. Biology, University of Nebraska at Omaha

    Research Interests:

    My research interests include studying how endogenous oxidized polyunsaturated fatty acid (PUFA) metabolites, also called oxylipins, affect age-associated neurodegenerative diseases. Throughout this work I will identify and study the corresponding mechanism of oxylipins that either accelerate or alleviate age-associated neurodegeneration, specifically the epoxy- and dihydroxy-metabolites of omega-3 (ω-3) and omega-6 (ω-6) fatty acids.

    Endogenous oxylipins are crucial in human and animal physiologies as they are involved in CNS and cardiovascular functions, inflammation, and tissue repair despite their low abundance. As well, recent studies have indicated that chronic metabolic and neurodegenerative diseases could significantly impact the endogenous oxylipin profile in target tissues and inhibiting the metabolism of specific oxylipins could be beneficial to these diseases. In addition, several recent studies show that the exposome, such as a fatty acid diet, environmental toxicants, and everyday products, can impact oxylipin metabolism. Thus, in this specific project, I hypothesize that changes in the oxylipin profiles in C. elegans due to the exposome or aging consequently affect age-associated neurodegeneration. However, investigating the crosstalk between oxylipin metabolism and age-associated neurodegeneration in mammalian models and humans is challenging owing to the length of the experiments and difficulties to control potential exposures that could affect oxylipin metabolism. Therefore, in my thesis project, I propose to conduct our study in the model organism Caenorhabditis elegans (C. elegans) as the neuron signaling and PUFA metabolism of humans are conserved in C. elegans, their transparent body facilitates fluorescence neuronal imaging assays, and their relatively short lifespan expedites aging studies compared to other biological models. As well, C. elegans are genetically malleable and their diet can easily be modified to introduce a variety of compounds or varying fatty acid concentrations.

    To test our hypothesis, we will analyze the oxylipin profile in C. elegans exposed to environmental toxicants at different ages to identify the oxylipins that are significantly impacted by exposome or aging. These identified oxylipins will then be supplemented to C. elegans allowing use to subsequently analyze how the exposome and aging affects neurodegeneration in C. elegans with phenotypic and morphological assays. By combining the results from these studies, we could delineate the mechanism behind how the exposome affects aging and age-associated neurodegeneration through PUFA oxylipin signaling pathways.

    Here I propose to use state-of-the-art oxylipin profiling and neuronal function assays to i) identify specific metabolic changes in abundance within the oxylipin profiles throughout the lifespan that may be involved in aging, ii) determine the effect (i.e., severity, motor neurons affected, changes in lifespan) of these identified metabolites on neurodegeneration and neurodegeneration recovery, and iii) investigate a possible mechanism of ferroptosis, an iron-dependent programmed cell death that is characterized by an accumulation of lipid reactive oxygen species, to be responsible for the metabolic changes over the lifespan further resulting in the observed neurodegeneration. Once I establish the methodology for my research, and along with the study of oxylipins, I will then investigate how common yet toxic compounds (i.e., pesticides, metals, over-the-counter drugs, and personal care products) can affect aging and neurodegeneration with sustained exposure through the oxylipin signaling pathway. With these projects, I hope to elucidate the mechanism and progression of neurodegeneration due to these differences in fatty acid levels and exposure to environmental toxic chemicals in C. elegans that could translate to neurological diseases in humans, such as Parkinson’s and Alzheimer’s diseases. If these studies exhibit promising results corresponding to a causal effect between oxylipins and neurodegeneration in C. elegans, further studies could be conducted in more sophisticated mammalian models to support these results.

    Major Professor: Kin Sing Lee, Pharmacology and Toxicology

    Contact: hinmanje@msu.edu

Comparative Medicine and Integrative Biology

  • Azam Ali Sher

    Azam SherCooperating Doctoral Program: CMIB

    EITS Track: Biomedical Toxicology

    Education: Doctor of Veterinary Medicine (D.V.M), University of Agriculture Faisalabad, M.S. Epidemiology, Michigan State University

    Research Interests:
    The emergence and global spread of antimicrobial resistance (AMR) among bacterial pathogens against life-saving drugs have become a major challenge for both public health and clinical settings. My focus of research is to understand the mechanistic role of the gut microbiome in the development and transmission of AMR in commensals and pathogenic bacteria, and also explore different dynamics of the gut microbiota pre and post antibiotic treatment. I am currently working on to build an in-vivo animal based system that mimics the human gut to address this complex scientific question by integrating different Omics and synthetic biological techniques. This study will lead us to uncover different drug-microbiome-host interactions and find some solutions to halt AMR in the gut and environment.

    Major Professor: Linda Mansfield, Large Animal Clinical Sciences, Microbiology and Molecular Genetics

    Contact: sherazam@msu.edu

  • Christine Wei

    Christine WeiCooperating Doctoral Program: CMIB

    EITS Track: Biomedical Toxicology

    Education: Biochemistry and Molecular Biology, Michigan State University

    Research Interests:

    Both chronic liver disease and acute liver injury can be induced by chemical exposures and in each context, the blood coagulation cascade is activated. Multiple studies suggest that components of the blood coagulation system modify the pathogenesis of acute hepatotoxicity and participate in the regeneration of the injured liver. My research is focused on defining the precise mechanisms linking the clotting protein fibrinogen to liver injury and repair. 

    After partial liver resection, the remaining liver regenerates, driven in part by hepatocyte proliferation, to restore normal hepatic functions. This surgical procedure is used to remove liver tumors and in the case of living donor liver transplantation. Interestingly, up to 10% of patients develop complications after partial resection. This can extend hospitalization time, and lead to serving complications including liver failure or death. After liver resection (partial hepatectomy, PHx), blood coagulation is activated, and fibrinogen is deposited in the liver. Prior studies suggest that failed hepatic fibrinogen deposition or low plasma fibrinogen after surgery is associated with post-operative liver dysfunction. Moreover, in the 2/3rd partial hepatectomy model in mice, fibrinogen depletion with ancrod significantly reduced hepatocyte proliferation. What’s more, prior studies also suggest the protein that degrades fibrinogen also contributes to hepatocyte proliferation, which further articulates the role of fibrinogen on hepatocyte proliferation. Although prior studies suggest that fibrinogen contributes to liver regeneration after PHx, the precise mechanisms are unclear. This is the focus of my research. 

    Major Professor: James Luyendyk, Pathobiology and Diagnostic Investigation

    Contact: weizimu@msu.edu

Fisheries and Wildlife

  • Janice Albers

    Janice AlbersCooperating Doctoral Program: Fisheries and Wildlife

    EITS Track: Environmental Toxicology

    Education: B.S. Water Resources Fisheries Option and Biology, University of Wisconsin - Stevens Point

    Research Interests:
    My research interests are to actively restore stream fish communities by researching new ways to apply individual-level parameters to predict and manage at the population scale in order to provide the most effective restorative management actions. One way to accomplish this goal is to assess risk from pollutants more efficiently using Adverse Outcome Pathways (AOP). Consequently, my dissertation topic is the 'Development of a neurobehavorial AOP for fish larva: incorporating ecologically relevant behavioral alterations for multiple species after exposure to PCB126 and methylmercury.'

    Major Professor: Cheryl Murphy, Fisheries and Wildlife

    Contact: albersja@msu.edu

Food Science and Human Nutrition

  • Ankita Bhattacharya

    Ankita BhattacharyaCooperating Doctoral Program: Food Science & Human Nutrition

    EITS Track: Food Toxicology & Ingredient Safety Track

    Education: B.S. Food Science & Technology, University of Delhi

    Research Interests:
    I graduated from the University of Delhi with a Bachelor of Science in Food Technology and experienced working with the Food and Drug Administration in India. Through that experience, I developed a keen interest in learning more about environmental contaminants in food and the creation of standards for the protection of public health. My research in the Carignan Lab combines food science with epidemiology, water quality, soil, and crop sciences to investigate exposure pathways for poly- and perfluoroalkyl substances.

    Major Professor: Courtney Carignan, Food Science & Human Nutrition, Pharmacology & Toxicology

    Contact: bhatta59@msu.edu

  • Ying Guo

    Ying GuoCooperating Doctoral Program: Food Science & Human Nutrition

    EITS Track: Food Toxicology & Ingredient Safety Track

    Education: B.S. Environmental Science, Northwest University, M.S. Food Science and Human Nutrition, University of Florida

    Research Interests:
    I’m interested in understanding exposure to environmental contaminants through dietary and environmental pathways. My thesis will focus on these pathways for perfluoroalkyl substances (PFAS) for a community impacted by PFAS contaminated drinking water in the context of a biomonitoring study.

    Major Professor: Courtney Carignan, Food Science & Human Nutrition, Pharmacology & Toxicology

    Contact: guoying4@msu.edu

  • Patricia Hsu

    Pin-Yi HsuCooperating Doctoral Program: Food Science & Human Nutrition

    EITS Track: Food Toxicology & Ingredient Safety Track

    Education: B.S. Public Health and Agronomy, National Taiwan University

    Research Interests:
    I have a great interest in studying the global risk assessment of mycotoxins, especially aflatoxin, among different countries. I am currently working with Dr. Felicia Wu on a project called, “Aflatoxin M1 Health Risks vs. Benefits of Dairy Consumption in Ethiopian Children: An Epidemiological Trial and Risk-Benefit Analysis.” In this project, our goal is to provide sound risk and epidemiological science to the question of aflatoxin M1 (AFM1) in dairy products: what its true health effects are, how any health risks compare to the nutritional benefits of milk
    consumption, and what the implications are for rational policymaking. Moreover, we hope to fill gaps in knowledge and policy surrounding aflatoxin M1.

    Additionally, my other research focus, “Sustainable, Systems-Based Solutions for Ensuring Low-Moisture Food Safety”, is mainly focusing on dealing the food recall problems of pathogenic bacteria (Salmonella) in low-moisture foods (almonds and raw flour). Through this study, based on the previous food recall cases that have occurred in the United States, we expect that
    food product recall cases could be reduced by the improved traceability system, which involved with optimisation and models development. Moreover, we hope to estimate the economic loss resulting from the recalls of these two food products, thereby preventing the food recalls from happening repeatedly in the future.

    Major Professor: Felicia Wu, John A. Hannah Distinguished Professor, Department of Food Science and Human Nutrition, Department of Agricultural, Food, and Resource Economics

    Contact: hsupin@msu.edu

  • Maria Kloboves

    Maria KlobovesCooperating Doctoral Program: Food Science & Human Nutrition

    EITS Track: Biomedical Toxicology Track

    Education: B.S. Animal Science, Michigan State University

    Research Interests:
    My research interests center around the intersection between nutrition, toxicology, and pregnancy. I have a particular interest in the relationship between maternal obesity and endocrine disrupting chemicals (EDCs) and their impact on the anogenital distance (AGD) and 2:4 finger digit ratio (2:4D) of the offspring. Obesity is a prominent condition in the United States and an alarming number of women begin pregnancy as obese. This presents problems for the offspring because maternal obesity has been linked to increased risk for development of metabolic diseases and reproductive disorders. In the past, AGD and 2:4D ratios have been used as indicators of reproductive function later in life. The hormonal shifts in testosterone and estrogen resulting from obesity may alter the AGD and 2:4D of offspring, thus potentially providing a window into in-utero development and early biomarkers of reproductive disorders.

    EDCs are near impossible to avoid and can be found in personal care products, cosmetics, plastics, and food wrappings. Recent studies with EDCs have shown that AGD and 2:4D reflect the uterine environment and could be useful in understanding the mechanisms and effects of EDCs and EDC alternatives on fetal development and maternal health. Ultimately, I would like to direct my research towards the interaction between hormones, EDCs, and women's health. Pregnancy is a critical period for both the mother and the fetus, but environmental factors- such as diet and chemical exposures- can have profound impact on a woman's health before and after pregnancy. Furthermore, the effects of these EDCs during pregnancy may contribute to the development of uterine fibroids, cardiovascular disease, and other health conditions.

    Major Professor: Rita Strakovsky, Human Nutrition

    Contact: kloboves@msu.edu

  • Diana Pacyga

    Diana PacygaCooperating Doctoral Program: Food Science & Human Nutrition

    EITS Track: Biomedical Toxicology Track

    Education: B.S. Molecular and Cellular Biology, Chemistry Minor, Neuroscience Certificate, University of Illinois at Urbana-Champaign

    Research Interests:
    My research interests combine human nutrition with population-based research and environmental health. My research, specifically, focuses on pregnancy as a critical time for maternal and fetal health. The primary objective of this research is to understand how prenatal exposures to environmental toxins found in a wide range of consumer products (e.g. food, personal care, and household products) and maternal lifestyle factors (e.g. maternal obesity and adiposity) affect pregnancy health and fetal development. The long-term goal of this research is to determine the mechanisms by which maternal lifestyle factors (e.g. environmental toxins and maternal obesity) affect pregnancy, birth, and childhood outcomes. The hope is to establish recommendations for pregnant women to prevent adverse outcomes associated with these lifestyle factors.

    Major Professor: Rita Strakovsky, Human Nutrition

    Contact: pacygadi@msu.edu

Forestry

  • Luis Rivera-Cubero

    Nikita Saha TurnaCooperating Doctoral Program: Forestry

    EITS Track: Environmental

    Education: B.S. Environmental Technology, University of Puerto Rico-Aguadilla

    Research Interests:
    How urban trees intercept airborne pollutants, the transport and fate of these pollutants in urban ecosystems.

    Major Professor: David Rothstein, Biochemistry & Molecular Biology

    Contact: riveracu@msu.edu

Microbiology and Molecular Genetics

  • Morgen Clark

    Morgen ClarkCooperating Doctoral Program: Microbiology and Molecular Genetics

    EITS Track: Environmental Toxicology

    Education: B.S. Molecular Genetics, University of Vermont

    Research Interests:
    My research in the Reguera lab investigates the mechanisms used by metal-reducing bacteria in the genus Geobacter to grow in environments impacted by metal contaminants. These bacteria show promise for clean-up efforts because they are able to grow and immobilize toxic metals and radionuclides. Furthermore, their growth and activity can be stimulated in situ by the addition of acetate, their preferred electron donor. My lab uses Geobacter sulfurreducens and other laboratory representatives of the environmental strains to gain fundamental insights into the physiological adaptations that allow these microbes to grow in the presence of metals at concentrations otherwise lethal to most other bacteria.

    I am particularly interested in further characterizing the conductive protein appendages (Type IV pili) that Geobacter cells assemble on the cell surface to bind and reduce toxic metals. Studies with uranium demonstrated that the pili bind the uranyl cation and reductively precipitate it outside the cell, simultaneously preventing it from traversing the cell envelope and providing energy for growth. Previous studies in my lab purified the pili and demonstrated they are protein nanowires. The team also resolved the structure of a pilus fiber via molecular dynamics and identified surface ligands that could function as metal-binding motifs and reductive sites for uranium and other cationic metals such as cobalt, gold, and silver. Additionally, my lab developed computational tools to design recombinant versions of the nanowire peptide (pilin) and assembled them in vitro into protein fibers with the same conductive properties as the native counterparts.

    My dissertation builds on these studies and aims to 1) resolve the structure of the conductive pili via cryo-electron microscopy (a collaboration with Dr. Kristin Parent in the department of Biochemistry and Molecular Biology) and 2) investigate the spectrum of metals that they can bind and reductively precipitate. I am particularly interested in cadmium (Cd), a metal contaminant that is persistent in agricultural soils and aquaculture systems. The solubility of the Cd2+ cation makes it highly mobile in soils and promotes its rapid uptake and concentration in plants, farmed animals, and shellfish. Cumulative exposure from these sources through dietary intake is prevalent and has long-term health consequences. Also of interest to food security is the fact that Cd, even when present in moderate and “safe” amounts, co-selects for metal and antibiotic resistance in foodborne pathogens. Cd also leaches rapidly in agricultural runoffs, increasing the risk of exposure and the selective pressure for “superbugs”. Yet Geobacter bacteria live in environments impacted by cadmium contamination, tolerate high concentrations of the mobile and toxic Cd2+. cation, and are known to contribute to its mineralization. This makes them great model systems to investigate how metal stressors contribute to the co-selection of antibiotic traits in microbial communities. Hence, my dissertation also includes a third aim that will investigate genomewide responses of Geobacter bacteria to Cd stress. The size, charge, and coordination of the pilus metal traps suggests that it can bind Cd2+, providing a biological mechanism for its reductive precipitation as Cd0. This reaction could help detoxify the metal, but it is at the thermodynamic edge and is therefore unlikely to generate energy for growth. Thus, yet unknown adaptive responses allow Geobacter cells to remain viable and metabolically active in environments impacted by Cd contamination.

    Major Professor: Gemma Reguera, Microbiology and Molecular Genetics

    Contact: clarkmo9@msu.edu

  • Joel Marty

    Joel MartyCooperating Doctoral Program: Microbiology and Molecular Genetics

    EITS Track: Biomedical Toxicology

    Education: B.S. Biomedical Sciences, Western Michigan University

    Research Interests:
    With the implementation of combined antiretroviral therapy (cART) HIV prognosis has shifted to a manageable chronic disease. However, as this population of people with HIV age there is a correlated increasein neuroinflammation, which may contribute to the pathogenesis of HIV associated neurocognitive disorders (HAND). CD8+T cells are capable of crossing the blood brain barrier and potentially contribute to this inflammation. My project will assess the immunopharmacological nad immunotoxicological effects of cannabinoid treatment, specifically THC and JWH-015 (a selective CB2 agonist), on primary human CD8+T cells. Once the immunopharmacological/immunotoxicological effects of the cannabinoid treatment have been determined we will develop a coculture of primary human astrocytes with the cannabinoid treated primary human CD8+T cells. 

    Major Professor: Norbert Kaminski, Pharmacology & Toxicology 

    Contact: martyjoe@msu.edu

Pharmacology and Toxicology

  • Saamera Awali

    Saamera AwaliCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. University of Detroit Mercy

    Research Interests: Nuclear factor erythroid 2-related factor (Nrf2) is a transcription factor that helps regulate antioxidant proteins involved in protection against oxidative and inflammatory stress. Studies show that Nrf2 demonstrates anti-inflammatory effects and plays a key role in decreasing susceptibility to chronic illnesses related to oxidative stress, thus it has been a therapeutic target of interest for several diseases. Data from our lab suggests that Nrf2 modulates T cell activation and CD8+ T cell effector function. Specifically, our lab has demonstrated that tBHQ, a potent Nrf2 activator, blunts the expression of CD107, a marker of T cell degranulation, on CD8+ T cells, suggesting that it impedes T cell activation and suppresses effector function. Although published data from our lab demonstrates a T cell autonomous role for Nrf2 in modulating T cell function, there is considerable evidence from other labs to show that Nrf2 also regulates antigen-presenting cells, such as dendritic cells. Notably, Nrf2 has been shown to regulate the T cell response by modulating dendritic cell activation induced by oxidative stress. In addition, it has been shown that dendritic cells lacking Nrf2 demonstrate increased expression of MHC class II, and the co-stimulatory molecules CD86, and CD80, which work jointly to promote T cell responses. Our hypothesis is that Nrf2 activation by tBHQ in dendritic cells will inhibit expression of MHC class II and other co-stimulatory molecules involved in effector functions, suggesting a blunted immune response after influenza infection. I intend to test this hypothesis in our mouse model of influenza and through the use of Nrf2-deficient models. I am concurrently developing in vitro assays to complement our in vivo approach.

    Major Professor: Cheryl Rockwell, Pharmacology and Toxicology

    Contact: awalisaa@msu.edu

  • Rachel Bauer

    Rachel BauerCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Food Toxicology & Ingredient Safety

    Education: B.S. Nutrition and Biology, Morgan State University

    Research Interests: My dissertation research will focus on characterizing exposure to PFAS chemicals and investigating impacts on immune function. I am currently involved with research that aims to quantify concentrations of PFAS in the body as well as in drinking water and other potential sources. Questionnaires are being administered to obtain information about participant demographics, diet, and habits. I will employ statistical models to determine relative contributions of exposure sources in relation to PFAS body burdens, and associations with measures of immune function. I will also use exposure models to reconstruct historic or current exposure from specific sources and calculate estimates of risk.

    Major Professor: Courtney Carignan

    Contact: bauerra2@msu.edu

  • Sierra Boyd

    Sierra BoydCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Neuroscience, Michigan State University

    Research Interests: My dissertation work in the laboratory of Dr. Alison Bernstein focuses on investigating how environmental toxicants increase risk of Parkinson’s disease (PD). Specifically, I focus on the organochlorine pesticide, dieldrin. Developmental exposure to dieldrin is known to induce a poised epigenetic state and to increase susceptibility to PD-related degenerative insults, possibly through alterations in dopamine (DA) packaging and neurotransmission. The Bernstein lab has developed a novel two-hit model of parkinsonian toxicity combining developmental dieldrin exposure with the α-synuclein pre-formed fibril model to study the mechanisms underlying this increased susceptibility. In my dissertation work, I will use this model to assess the effect of dieldrin on PFF-induced deficits in DA neurotransmission and packaging in the striatal DA terminals by using fast-scan cyclic voltammetry and radioactive vesicular uptake. In addition, I will be using 3D Lund Human Mesencephalic cells, a DA neuron cell culture model, to determine the mechanisms by which genes with dieldrin-induced epigenetic alterations affect neuronal function and susceptibility to PD-related degenerative insults.

    Major Professor: Alison Bernstein, Translational Science and Molecular Medicine

    Contact: boydsier@msu.edu

  • Devon Dattmore

    Devon DattmoreCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Biology/Biochemistry, State University of New York at Cortland

    Research Interests: I am interested in how dietary fats and their downstream metabolites modulate insulin signaling. There are evidence suggesting that certain fats may be beneficial in facilitating improved insulin signaling, whereas other fats seem to impair insulin signaling. Long term impairment of insulin signaling results in insulin resistance (IR), which may progress into type II diabetes mellitus. While much investigation has been conducted assessing the contributions of saturated fat, not as much is known about the contributions of polyunsaturated fats (PUFAs) and even less is understood regarding PUFA epoxy-metabolites (EpPUFAs). This is due in part to the difficulty of studying supplementation in mammalian models as well as cell culture. Mammals cannot synthesize PUFAs, and so they must obtain these fats from dietary sources. Furthermore, levels can vary due to quantities and durations of intake. Interestingly, there is a species of nematode, Caenorhabditis elegans (C. elegans), which have the capacity to produce PUFAs/ EpPUFAs endogenously by a pathway that is nearly identical to mammals (and humans). What is more, their insulin signaling pathway is evolutionarily conserved. Lastly, there are knock-out mutant worms available, which lack the abilities to synthesize particular PUFAs/ EpPUFAs. Thus, my dissertation research seeks to establish C. elegans as a model organism for assessing the differential effects of PUFAs and their epoxy-metabolites on IR under high-glucose conditions, as well as determine the receptor for one of the EpPUFAs (epoxy-eicosatrienoic acid) which has been shown to be beneficial in treating insulin resistance in mammalian models. This research is important to the field of toxicology, because some environmental xenobiotics have been demonstrated to alter EpPUFA metabolism (such as trichlocarbon), hence an established understanding of how altered EpPUFA metabolism affects insulin signaling in C. elegans may provide useful insights as to how particular xenobiotics might contribute to insulin resistance in mammals.

    Major Professor: Kin Sing Stephen Lee, Pharmacology & Toxicology

    Contact: dattmore@msu.edu

  • Olivia Favor

    Vanessa BenhamCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Biochemistry and Molecular Biology, Michigan State University

    Research Interests: My overarching research interests include pathogenesis of autoimmune disease, regulation of cytokine signaling, and biochemical physiology. My dissertation topic revolves around studying the attenuation of lipopolysaccharide (LPS)-induced NLRP3 inflammasome activation in murine alveolar macrophages by administration of polyunsaturated fatty acids (PUFAs), epoxygenated fatty acids, (EpFAs) and soluble epoxide hydrolase (sEH) inhibitors, including 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU). NLRP3 inflammasome activation in alveolar macrophages has been shown to potentiate widespread systemic inflammation in both mice and humans by generating large quantities of pro-inflammatory cytokines (i.e., IL-113 and IL-17), ultimately leading to the pathogenesis of autoimmune systemic lupus erythematosus (SLE).

    Currently, I am studying pro-inflammatory, anti-inflammatory, and cytotoxic effects of 14 EpFAs in the absence and presence ofTPPU in vitro, using the RAW 264.7 cell line. In the future, I am interested in studying the anti-inflammatory effects of administering a DHA-rich diet and TPPU to
    NZBWF1 mice (a lupus-prone strain) and determining whether or not DHA supplements and TPPU should be coupled to provide a more effective therapeutic option for SLE. I am also interested in identifying targets of EpFAs in RAW 264.7 cells and studying their downstream effects on transcription of cytokine precursors, specifically in regard to nuclear factor kappa 8 (NF-KB) and peroxisome proliferator-activated receptor (PPAR) signaling.

    Major Professor: Kin Sing Lee, Pharmacology & Toxicology

    Contact: favoroli@msu.edu

  • Brianna Finn

    Cooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Biochemistry, Michigan State University

    Research Interests: Immunopharmacology/immunotoxicology of cannabinoids. Dissertation project will be in this general area, but the specific aims of the project will be determined in the near future.

    Major Professor: Norbert Kaminski, Pharmacology & Toxicology

    Contact: finnbri1@msu.edu

  • Romina González-Pons

    Cooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Natural Sciences with a concentration in Biology, University of Puerto Rico at Cayey

    Research Interests: Liver health is profoundly influenced by hepatic immune homeostasis. Evidence suggests that dysregulation of the hepatic immune system aggravates liver disorders such as acute liver failure (ALF). ALF can arise as a consequence of acetaminophen (APAP) overdose, which is the most common cause of ALF in the United States. Recent data from our
    laboratory demonstrate that after an initial hepatic insult by APAP, monocyte-derived macrophages (MDMs) are recruited to the site of injury where they initiate tissue repair. Under conditions of severe liver injury, however, MDMs become dysregulated and contribute to the progression of ALF. This results in the amplification of pro-inflammatory cytokines, including IL-6 and TNF alpha, which contribute to the systemic inflammation culminating in hepatic encephalopathy (HE; i.e., cognitive impairment) and multi-organ failure. The current treatment for APAP-induced hepatotoxicity is Nacetylcysteine (NAC). However, the efficacy of NAC is poor when administered beyond eight hours of APAP overdose. ALF patients often rely on liver transplantation (LT) as their only therapeutic option. LT may not be sufficient, however, if ALF patients present with severe HE. Despite the increasing knowledge in the field, the mechanisms whereby MDMs become dysregulated are incompletely understood. My research focuses on elucidating the mechanisms whereby MDMs become dysregulated and contribute to the sustained hepatic inflammation and HE in APAP-induced ALF. Understanding these mechanisms could provide critical insight into novel therapeutic targets to treat ALF patients.

    Major Professor: Bryan Copple, Pharmacology & Toxicology

    Contact: gonza737@msu.edu

  • Lauren Heine

    Cooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Biology, University of Hawaii at Manoa

    Research Interests:
    My dissertation project will explore the hypothesis that dietary omega-3 fatty acid supplementation can aid in reducing the amount of glucocorticoids (GCs) required to suppress environmental toxicant-triggered flares and progression of systemic lupus erythematosus (SLE). Currently, GCs are one of the most commonly used treatments for SLE. Prolonged usage of GCs, however, can lead to life-threatening side effects such as cardiovascular disease, osteoporosis, infection, hypoglycemia and myopathy. It has been previously shown that many of the innate and immune pathways associated with SLE can be regulated by not only GCs but also dietary supplementation with omega-3 fatty acids. Therefore, given this overlap, we want to determine whether dietary omega-3 supplementation may have GC-sparing effects that provides SLE patients with a safer, less toxic, and effective long-term treatment. 

    The two main aims of my project are to: 1) evaluate how docosahexaenoic acid (DHA; a widely used omega 3 fatty acid supplement) influences dose-dependent effects of the GC prednisone in silica-triggered autoimmunity and nephritis in mice, and 2) determine how DHA alters the effects of prednisone in regards to silica triggering of long-term autoimmune progression, kidney injury and overall survival. These specific aims will be tested using female NZBWF1 lupus-prone mice instilled with crystalline silica (cSi)2; trigger for lupus) to model the environmentally-triggered flares and progression of SLE. We will also conduct in vitro studies to determine the anti-inflammatory effects of dexamethasone (another commonly perscribed GC) in RAW 264.7-ASC cells and MPI cells.

    Major Professor: Jack Harkema, Pathobiology & Diagnostic Investigation

    Contact: heinelau@msu.edu

  • Amanda Jurgelewicz

    Amanda JurgelewiczCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Biochemistry & Chemical Biology, Wayne State University

    Research Interests:
    2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant that has been associated with a variety of adverse health effects. Its toxicity is elicited through binding to the aryl hydrocarbon recpetor (AhR) in the cytoplasm of the cell. This complex will translocate to the nucleus and dimerize with the aryl hydrocarbon nuclear transporter (ARNT) permitting binding to DNA that will lead to changes in gene expression. TCDD exposure has been linked to susceptibility to developing metabolic syndrome, but the mechanism for how TCDD is disrupting basic metabolism is largely unknown. This disruption can lead to changes in cholesterol homeostasis, as TCDD induces a down-regulation of HMG-CoA-reductase (HMGCR) that is necessary for the rate limiting step of cholesterol biosynthesis. TCDD exposure can also induce hepatic steatosis in mice, which is one of the early stages of non-alcoholic fatty liver disease (NAFLD). Recent studies have suggested a strong link between changes in cholesterol homeostasis and the development of NAFLD. My research will be focused on determining the mechanistic link between AhR-mediated signaling, cholesterol metabolism and TCDD-induced liver injury. The impact of simvastatin, a HMGCR inhibitor, will also be explored.

    Major Professor: John LaPres, Biochemistry & Molecular Biology

    Contact: jurgelew@msu.edu

  • Dawn Kuszynski

    Dawn HenderlongCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxciology Track

    Education: B.S. Cell and Molecular Biology, University of Michigan

    Research Interests:
    I am interested in researching drugs to prevent/treat cardiovascular diseases. Currently in Adam Lauver's lab I am studying a novel conjugate of clopidogiel, DT678, in rabbits. We test for both its efficacy and safety compared to other clinically available antiplatelet therapies. A major problem with current antiplatelet drugs are the bleeding side effects. I hope to elucidate some of the causes for these bleeding tendencies so that new drugs can be developed that have an increase in safety compared to older drugs.

    Major Professor: Adam Lauver, Pharmacology and Toxicology

    Contact: henderl7@msu.edu

  • Omar Kana

    Omar KanaCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Biochemistry, Louisiana State University

    Research Interests:
    My primary interest is in bioinformatics, and its applications in toxicology. Specifically, I plan to work in understanding global mechanisms of gene regulation in the liver and their perturbation under exposure to toxicants. My current project uses statistical learning tools that I am developing to predict and elucidate the regulation of cytochrome p450's in the human liver. Our goal is to improve understanding of the drug pharmacodynamics in the human liver, adverse drug reactions, and at risk populations for drug-induced and environmental toxicity. 

    Major Professor: Sudin Bhattacharya, Biomedical Engineering, Pharmacology and Toxicology

    Contact: kanaomar@msu.edu

  • Isha Khan

    Isha KhanCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: Bachelor of Pharmacy, University of Dhaka

    Research Interests:
    I am working at the preliminary stages of my research project. My project would focus on investigating the role of dioxins in the regulation of hematopoietic stem cell development into lymphocytes that commit to the B cell lineage. Dioxins are persistent environmental pollutants that are byproducts of industrial manufacturing processes. Studies by a previous graduate student showed that 2,3,7,8-tetrachlorodibenzo-p-dioxin, the most toxic of dioxins, accelerates the loss of the stem cell phenotype by binding to the aryl hydrocarbon recpetor (AhR) but then the developing cells arrest prior to becoming fully committed B cells. This observation is consistent with a study from another laboratory, which reported that AhR antagonists maintain hematopoietic stem cells in a stem-like phenotype. Another critical observation by the same prior graduate student that would be a jumping off point for my dissertation studies involves suppression by AhR antagonists of early B cell factor-1 (EBF-1), a transcription factor that is essential for B cell lineage commitment. The promoter for EBF-1 has 13 elements to which the AhR can bind, termed dioxin-response elements or DRE. Several of these binding sites have been confirmed by electrophoretic mobility shift assays, many of which overlap the binding motif of another transcription factor involved in B cell development termed PAX5. My project would involve continuing the elucidation of how dioxins can influence B cell development through the AhR receptor.

    A major focus of my laboratory study, which is related to the project above, has been characterizing the human pro-B cell line, JM-1 cells, which do not express the aryl hydrocarbon receptor but have been genetically modified to express the aryl hydrocarbon receptor gene, JM-1 AhR+ cells. During my time at the laboratory, I have been investigating the level of aryl hydrocarbon receptor in the JM-1 AhR+ cells and confirming whether the JM-1AhR+ cells possess a functional aryl hydrocarbon receptor. The JM-1AhR+ cells would be a very useful model to study how dioxins can alter the B cell developmental process.

    Major Professor: Norbert Kaminski, Pharmacology and Toxicology

    Contact: khand@msu.edu

  • Jessica Moerland

    Jessica MoerlandCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Human Biology, Michigan State University

    Research Interests: I am primarily interested in the links between inflammation and cancer. I am interested in how malignant cells and immune cells interact within the tumor microenvironment of lung, breast, and pancreatic cancer, and how we can modulate those interactions pharmacologically to help prevent or treat cancer. Currently, I am focusing on two targets for anti-cancer pharmacological intervention: the Nrf2 cytoprotective pathway and the RXR nuclear receptor. 

    Major Professor: Karen Liby, Pharmacology & Toxicology

    Contact: moerlan2@msu.edu

  • Ebenezar Okoyeocha

    Ebenezar OkoyeochaCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.MLS. Medical Laboratory Science, University of Nigeria, Nsukka

    Research Interests: My research interest is to elucidate the mechanism of chemical induced injury, and identify targeted treatment options.

    Current study: Chloropicrin (Trichloronitromethane, CP), a toxic agent used during World War 1 as a warfare agent, is currently been used as a soil fumigant and pesticide. It is volatile and easily accessible, and this increases the probability of accidental and occupational exposure to CP, as well as its use in terrorism. Exposure to CP results in severe ocular injury, especially to the corneal. However, the mechanism of its injury is not well defined hence, treatment options are limited. Studies in our laboratory using human corneal epithelial (HCE) cells and ex vivo rabbit corneas suggests that GP-induced corneal pathogenesis is associated increased levels of nuclear erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (H0-1 ), a critical target enzyme downstream of Nrf2, suggesting that the Nrf2 pathway, a key antioxidant and cytoprotective system, could be activated following CP exposure. My current study in Dr. Neera Tewari-Singh's lab is focused on establishing an in vivo mouse ocular injury model with CP. I will further define the role of the Nrf2 pathway in GP-induced ocular injury using Nrf2 knockout (KO) mice. As part of our lab's novel therapeutic approach, I will be employing Nrf2 activators alone or in combination with SSOE in the treatment of GP-induced ocular injury. I propose that understanding the role of Nrf2 pathway in vivo is a critical first step in identifying targeted therapy.

    Major Professor: Neera Tewari-Singh, Pharmacology & Toxicology

    Contact: okoyeoch@msu.edu

  • Brad Ryva

    Bradley RyvaCooperating Doctoral Program: Pharmacology & Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Molecular and Cellular Biology, University of Illinois, Urbana-Champaign

    Research Interests:
    My research interests integrate toxicology, environmental health, women’s health, and medicine. Specifically, my research focuses on potentially modifiable lifestyle exposures and nausea and vomiting during pregnancy (NVP). One particular exposure of interest is endocrine disrupting chemicals (EDCs) found in many consumers products, such as food packaging materials and cosmetics. In addition, I will characterize the associations between these same exposures and gestational hormones, potentially providing insight into possible biological pathways that are currently weakly understood in humans. The long term goal of my research is understanding the role EDCs play in NVP and possibly providing clinical knowledge on modifiable risk factors. My project will bridge environmental toxicology and epidemiology by synthesizing tools from both fields, hopefully leading to novel insights into the role endocrine disruptors play in common pregnancy symptoms.

    Major Professor: Rita Strakovsky, Human Nutrition

    Contact: ryvabrad@msu.edu

  • Sera Sermet

    Sera SermetCooperating Doctoral Program: Pharmacology and Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Neuroscience, Michigan State University

    Research Interests:
    With the development of anti-retroviral therapy (ART), HIV has become a more manageable disease. This new treatment has successfully extended the life expectancy of the those afflicted with HIV to a life span comparable to a healthy individual. However, new problems arise as individuals live longer with HIV, such as development of HIV-associated neurodegenerative disease (HAND). Today, many individuals with HIV use cannabis to cope with side effects associated with the ART drugs. Previous research in the literature has shown that individuals with HIV who use cannabis have a decreased incidence of HAND development. My research will focus on elucidating the molecular mechanism of how cannabinoids induce their immunotoxicological and immmunopharmacological effects on the human immune system in the context of HIV. 

    Major Professor: Norbert Kaminski, Pharmacology & Toxicology

    Contact: sermetse@msu.edu

  • Michelle Steidemann

    Michelle SteidemannCooperating Doctoral Program: Pharmacology and Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Biology Microscopy Option, Central Michigan University

    Research Interests:
    2,3,7,8 tetrachlorodibenzo-ρ-dioxin (TCDD) is a persistent environmental toxicant that can cause cloracne, immune system depression, and metabolic diseases upon exposure. Classically the toxicity of TCDD has been thought to be mediated by a nuclear pathway in which TCDD binds to its endogenous transcription factor receptor, the aryl hydrocarbon receptor (AhR), in the cytoplasm of the cell. This complex can then alter gene transcription after translocating to the nucleus. There is evidence now, however, that suggests that the AhR might also have direct contact with mitochondria. The goal of my research will be to examine the interaction of the AhR and associated proteins with mitochondrial components such as the electron transport chain and mtDNA to try to determine if TCDD and other ligands are eliciting action through this organelle. These studies could provide insight into the development of the metabolic diseases caused by TCDD and even how endogenous ligands could be controlling mitochondrial function.

    Major Professor: John LaPres, Biochemistry and Molecular Biology

    Contact: steidem1@msu.edu

  • Nat Yawson

    Nat YawsonCooperating Doctoral Program: Pharmacology and Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Biochemistry, Kwame Nkrumah University of Science and Technology

    Research Interests:
    Visceral obesity increases the risk for both pre- and post-menopausal estrogen receptor positive breast cancer and pre-menopausal triple negative breast cancer (TNBC), however the mechanism has not been fully elucidated. Moreover, TNBC is the most aggressive and difficult breast cancer type to treat, with no current means of prevention. Our laboratory’s previous studies demonstrated that fibroblast growth factor-2 (FGF2) is released from visceral adipose tissue
    (VAT) and promotes mammary epithelial cell malignant transformation through the fibroblast growth factor-1 receptor (FGFR1). As part of my training in pharmacology and drug discovery, I worked with Bernard lab members to use our novel high throughput screen (HTS) to identify MSU generated terpenoids and cyclic peptides that inhibit FGF2-stimulated malignant transformation. These compounds were generated in collaboration with Drs. Richard Neubig, Edmund Elsworth, Johnathan Walton and Bjoern Hamberger (MSU). In this unique chemoprevention HTS,
    non-tumorigenic cells are stimulated to undergo anchorage-independent growth, a model of malignant transformation. Using this platform and anchorage-independent growth in soft agar, I confirmed that four terpenoids prevented FGF2-stimulated transformation. I propose to narrow  down compounds based upon safety and efficacy and test these natural products in vivo as chemopreventive agents. Moreover, I wish to understand their mechanisms of action. I hypothesize that VAT secretes FGF2 and induces downstream signaling driving mammary carcinogenesis and this can be prevented with natural products. This project will take the early steps to identify chemopreventive agents against breast cancer when VAT is a threatening risk factor.

    Major Professor: Jamie Bernard, Pharmacology and Toxicology

    Contact: yawsonna@msu.edu

  • Erin Zaluzec

    Erin ZaluzecCooperating Doctoral Program: Pharmacology and Toxicology

    EITS Track: Biomedical Toxicology

    Education: B.S. Chemistry, Michigan State University

    Research Interests:  Breast cancer is one of the top most diagnosed cancers and is the second leading cause of cancer death for women in the United States. Current approved preventative strategies include tamoxifen and raloxifene, two anti-estrogen treatments with adverse side effects that deter women from taking or completing the 5-year minimum requirement for risk reduction. Prophylactic mastectomy has up to a 90% risk reduction, but this invasive procedure has life-changing consequences at the physical, emotional, psychological, and social levels, therefore there is a need for development of new strategies for primary breast cancer prevention. 

    I am interested in novel approaches for primary breast cancer prevention through intraductal delivery methods. This approach allows for direct targeting of epithelial cells from which most breast cancers arise. Under the guidance of Lorenzo Sempere, I am investigating improved formulations for 70% ethanol; a cell-killing solution that completely ablates the ductal tree but has collateral tissue damage in the surrounding stroma. I am also investigating a less aggressive solution using CRISPR/cas9 technology to genetically edit mammary epithelial cells as an alternative prevention for estrogen receptor positive breast cancers. The two main aims of this project are to: 1) evaluate the genetic editing efficiency of this approach using immortalized and cancerous mammary epithelial cells lines of both mouse and humans, and 2) determine the feasibility of this approach in precancerous mouse and rat breast cancer models.

    Major Professor: Lorenzo Sempere, Radiology

    Contact: zaluzece@msu.edu

Plant, Soil and Microbial Sciences

  • Xu Zhiliang

    Cooperating Doctoral Program: Plant, Soil and Microbial Sciences

    EITS Track: Environmental Toxicology

    Education: B.S. Environmental Sciences / B.A. Chemistry, University of Iowa

    Research Interests:  My research program is to study uptake and accumulation of poly- and perfluoroalkyl substances (PFASs) and pharmaceuticals and personal care products (PPCPs) in the agricultural food crops. These emerging chemicals are frequently present in biosolids derived from wastewater treatment plants (WWTPs). The land application of biosolids to agricultural land as soil amendments and plant fertilizers could bring PFASs and PPCPs into soils, which could subsequently enter food crops and accumulate in the edible parts. Consumption of PFASs- and PPCPs-contaminated food crops can result in some adverse health problems to humans, especially to toddlers and children. Specific to my research, I will determine PFASs and PPCPs in biosolids samples collected from the WWTPs across the U.S., and achieved grain samples produced from the lands that had received the repeating applications of biosolids. In addition, I will conduct greenhouse experiments to examine how much PFASs and PPCPs will be accumulated in several agricultural food crops from the soils amended with biosolids. These research studies are essentially needed, because this information will be beneficial to estimating the health risk of humans after eating the crops grown in the biosolids-amended soils.

    Major Professor: Hui Li, Plant, Soil and Microbial Sciences

    Contact: xuzhilia@msu.edu